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Traumatic spinal cord injury 179Imaging EvaluationThe initial computed tomography (CT) scan obtained within2 hours of the fall showed ﬁndings of early diffuse cerebraledema, SDH, and SAH, including a prominent left parietalfocus of SAH and a focal right frontal SDH (Fig 1). A muchsmaller SAH/SDH were also present along the convexities,falx (ie, interhemispheric), and tentorium. There was no ev-idence of brain hemorrhage. No scalp or skull abnormalitieswere identiﬁed, although 1 observer could not rule out a“healed” skull fracture along the sutures in the parieto-occip-ital region. A CT scan performed 5 hours later showed pro-gression of the cerebral edema and no change in the SAH orSDH (Fig 2). A CT scan of the cervical spine was negative(Fig 3). Magnetic resonance imaging was recommended butnever obtained. A skeletal survey showed anterior wedge-likevertebral body deformities from T5 through T12 and inferiorL2. Some widening of the cranial sutures was present, but nofractures were conﬁrmed on the plain radiographs. The re-mainder of the survey was negative. A postmortem CT scan ofthe entire spine (Fig 4), conﬁrmed the vertebral deformities. Figure 2 A CT scan performed 5 hours after the initial CT scan shows marked progression of cerebral edema with complete loss of gray/Autopsy Findings by the Medical Examiner white matter differentiation, obliteration of sulci, and near complete obliteration of the ventricular system. A SAH is seen within com-Head and Brain pressed sulci in the left parietal lobe.A focus of hemorrhage was present in the left posteriorparietal scalp (ie, impact site). Microscopy showed acutehemorrhage with acute vital reaction within the ﬁbrousconnective tissue of the galea in that region. Brain weight axonal injury (TAI) observed microscopically on beta-was 1,270 g with the spinal cord attached. No skull frac- amyloid precursor protein (B-APP) immunoperoxidaseture was shown. The brain was extremely swollen with stains. There were bilateral, holohemispheric, thin-layergeneralized ﬂattening and ablation of the normal gyral SDHs with no mass effect.pattern. Histologically, a diffuse axonal injury pattern con-sistent with HIE was present. There were no gross trau-matic brain parenchymal injuries (eg, no contusion orshear lesions) or any histological evidence of traumaticFigure 1 A nonenhanced CT image of the brain preformed within 2hours of the fall shows decreased differentiation of gray/white mat- Figure 3 Sagittal reconstructed CT image of the cervical spine showster representing edema. normal alignment and no fractures.
180 Barnes et al Biomechanical Analysis A court-approved, biomechanical evaluation was performed including an investigation of the home setting where the injury reportedly occurred. A number of potential accidental and NAI (including SBS) scenarios were considered and an- alyzed primarily to address the thoracic spinal injuries and secondarily to address the cervical cord injury. The approach to the biomechanical analysis was to assume that the care- taker’s history was truthful and accurate and to then apply the principle of mechanics to evaluate whether or not such a history could be consistent with the subsequent injuries. This approach was not intended to rule out other possibilities but simply to evaluate the history provided. In that light, the caretaker consistently reported to all au- thorities that he had his back turned at the time of the inci- dent but that the boy had been standing up on the seat of the chair. He then reported hearing a noise and turning to ﬁnd the boy and the chair on the ﬂoor, with the chair lying on its back. Using the caretaker’s consistent history as one scenario,Figure 4 Sagittal reformation of the thoracic spine from a postmor- along with the imaging and clinical ﬁndings, the child wastem CT scan shows multilevel anterior wedge compression fractures assumed to have fallen, rotating with the chair until a point ofof varying degrees. separation (Fig 6). From that point, it was further assumed that he fell freely to strike the ﬂoor ﬁrst with his head and then with his dorsal neck and a shoulder, again based on theNeck and Spinal Cord imaging and autopsy ﬁndings. This “impact” scenario wouldFocal soft-tissue hemorrhages were present in relation to theright posterior neck and shoulder regions as well as the pos-terolateral transverse processes of the atlas and axis and at theC1-C2 intervertebral junction. No vertebral artery abnormal-ity was noted. The dura appeared tense and ﬁlled with blood-stained ﬂuid. Sagittal sections at the cervicomedullary junc-tion showed partial transection and disruption of the centralcord immediately distal to the inferior medullary olives. Thetissue appeared elongated and physically separated suggest-ing axial tension of the cord (Fig 5). The cellular responseconsisted of round and polymorphonuclear cells with acute,focal hemorrhage. Findings of ischemic neuronal degenera-tion were most prominent in, and adjacent to, the dorsal andventral neurons and consisted of cytoplasmic swelling, de-granulization, loss of ﬁne detail, and nuclear pynknosis.EyesOn gross examination, the pigmented layer of the retina wasfocally separated from the choroid. RHs were present primar-ily in the ganglion cell layer anteriorly but extended posteri-orly. An optic nerve sheath hemorrhage was also presentbilaterally. There was no mention of perimacular folds.Vertebral ColumnThe vertebral bodies from T2 through L3 to 4 were removeden bloc. A hemorrhage was seen in the anterior and lateralperivertebral ﬁbroconnective tissues. Microscopic sectionsshowed acute hemorrhage with ﬁbrin deposition replacingnormal marrow of all vertebral bodies. Multiple areas of dis-rupted cancellous bone with acute-phase osteogenic granu- Figure 5 A histological specimen through the cervicomedullarylation tissue were especially prominent T7 through T10. No junction shows complete disruption of the central cord elementscallus or osteoblast activity was present. (circle). (Color version of ﬁgure is available online.)
Traumatic spinal cord injury 181 34 in), his mass (15.9 kg, 35 lb), and the position of his CG being at approximately 57% his height,7 were used to deter- mine the CG of the combined system (Appendix 1). Thus, the ﬁrst phase of the fall was modeled with the child and chair combined as an inverted pendulum until the chair reached its natural tipping angle. Vertical and rotational velocities at this point were then used for the initial conditions of the subse- quent free fall, resulting in a predicted impact velocity rang- ing from 3.7 to 4.0 month(s). Impulse momentum was then applied to determine the severity of a fully plastic impact, modeling the child as a single spring-mass system, with the ﬂexing spine serving as the spring, and the mass deﬁned as the measured mass of the child minus that of his head. Be- cause there are limited data available to deﬁne an appropriate impact duration, a broad range of 50 to 100 milliseconds wasFigure 6 A schematic representation of the fall. (Color version of considered. Thus, the peak impact force was estimated toﬁgure is available online.) range between 0.9 and 1.9 N. A free-body diagram of the ﬂexed body was used to determine associated peak thoracic vertebral body forces ranging from 1.4 to 3.1 kiloNewtonsproduce ﬂexion and axial compression with the center of (kN). Forces in the separately considered head impact weremass of his body trailing above. The initial motion of the estimated to be between 3.4 and 3.7 kNs.child was assumed to have produced an initial rotation of thechild and chair together as an inverted pendulum systemabout an axis at the base of the chair’s rear legs. Once the Discussionchair reached its natural tipping angle, however, it was as-sumed to continue in its inverted pendulum motion while NAI/SBSthe child then fell freely to the ﬂoor. In this case, the initial “diagnosis” of NAI/SBS was based on Multiple anterior compression fractures of the thoracic the heretofore classic “triad” of SDH, RH, and encephalopa-spine, as reported in this case, are uncommon. The mecha- thy, along with a history presumed to be inconsistent withnism most consistent with this type of injury, however, the injuries. Central nervous system ﬁndings that mimic NAI/would be severe ﬂexion and/or axial compression of the SBS have been reported in accidental trauma and in a numberspine. It is problematic, biomechanically, to conclude that of medical conditions.14-21 The latter includes infection, co-such an injury can result from “SBS,” particularly in a child of agulopathy, metabolic disorders, and others.19-21 More recentthis age and size. Further evidence of head and shoulder reports also show that there is no speciﬁc pattern of intracra-impact suggests that the necessary loading of the spine may nial hemorrhage that is diagnostic of NAI/SBS to includehave been produced by forces applied to the head, neck, interhemispheric SDH and mixed-density SDH.14-17 Further-and/or shoulder. Thus, we chose to evaluate a scenario in more, recent evidence-based medical reviews (and legal chal-which the boy somehow caused the chair to tip. He then lenges) of the past NAI/SBS literature reveal that the vastrotated with the chair and ultimately fell in such a way that majority of these publications failed to achieve quality ofhis head struck the ﬂoor ﬁrst and quickly rotated to produce evidence ratings that would merit the use of the “triad” as aﬂexion in the neck and bring the shoulder/lower neck region standard or guideline for proof of NAI/SBS.1-8into contact with the ﬂoor. The force acting through the This case also shows the complexities involved in estab-shoulder area then acted to bring the remainder of the child’s lishing the sequence of injuries given multiple ﬁndings. Al-body mass to rest, resulting in ﬂexion and axial compression though initial concern for NAI is important and must beof the middle and lower spine. There are clearly many vari- reported, medical personnel must carefully correlate suchables associated with the chosen scenario, including the in- ﬁndings with the history to establish a correct sequence ofﬂuence of body rotation and whether the child was rotating events, including predisposing factors.19-21 The initiation offorward or backward, but there is no reason to believe the fall the criminal process before a complete and thorough childcould not have occurred as described. Given the selected protection and medical evaluation can lead to a rush in judg-scenario, the next step was to evaluate whether or not the ment. The injuries in this particular case were attributed toforces associated with the respective impacts to the head and SBS before the brain and spinal cord injuries were completelyshoulder/lower neck could have been severe enough to pro- evaluated.22 The father of the victim was charged with fatallyduce the injuries. shaking the child. After all the forensic evidence was consid- Analysis of the chair provided a seat height of 43 cm (17 in) ered, the ultimate verdict was acquittal.and a rearward tipping angle of 23°. The mass of the chair Given the fact that the law requires physicians to reportand its center of gravity (CG) were taken as equal to 6.8 kg suspected NAI, there is the danger of assuming NAI in all(15 lb) and the height of the seat, respectively. The chair cases of SDH and RH. As a result, further medical and imag-measurements, coupled with the height of the child (86 cm, ing workup may not be pursued (eg, magnetic resonance
182 Barnes et alimaging of the brain and cervical spine). The American Acad- Impact Injuryemy of Pediatrics, as others, strongly endorse the use of mag- Although there are no data available deﬁning skull fracturenetic resonance imaging in cases of suspected NAI.17,20,21,23 In thresholds (as an indicator of impact) for a 21-month-old,the absence of an apparent cause of diffuse cerebral edema data reported for younger infants33-36 and adults37 suggest(including HIE), cervical cord injury should be considered. that the calculated head-impact forces are enough to result inAfter the initial CT scan, magnetic resonance imaging is the fracture in at least some of the population. The absence ofchoice for delineating spinal, paraspinal, and intraspinal in- evidence of “signiﬁcant” trauma to the scalp and skull mayjury. A short tau inversion recovery (STIR) sequence should additionally be explained by the wide distribution of thealways be included because this technique provides the best force along the head, neck, and shoulders at the time ofsensitivity for these types of injury.21 impact. In young children with impact injury, there may be no focal scalp injury or skull fracture on physical examina-SCIWORA tion or by imaging. Therefore, the lack of such ﬁndings should not be interpreted as absence of impact injury. Addi-SCIWORA is not uncommon in toddlers and has been re- tionally, fatal and otherwise signiﬁcant intracranial injuriesported to occur after minor accidental trauma as well as in have been reported from accidental household or short fallscases of alleged NAI.13,24-29 Evidence of a spinal cord injury resulting in the triad of SDH, RH, and encephalopathy.38,39plus cranial, neck, and shoulder impact on the postmortem The biomechanical literature suggests different thresholds forexamination are the key ﬁndings in this case. The gross and central nervous system injuries given various scenarios.40-43histological ﬁndings, as well as the imaging ﬁndings, are en- Neck and cervical spine tissues may have a lower thresholdtirely consistent with the caretaker history of a household fall than brain for minimum forces required to produce trau-as corroborated by the biomechanical evaluation. This is true matic injuries.40for both the primary injury (ie, cord transection) and thesecondary injury (ie, HIE) as reﬂected in the clinical course ofthe child. SDH and SAH The bony structures of the cervical spine in infants and There are a number of potential causes for the SDH/SAH inyounger children are not fully developed as compared with this case. These include impact trauma, coagulopathy, in-that of the adult. Such “immaturity” includes the horizontal creased ICP, ischemic endothelial damage, and reperfusion.nature of facet joints with ﬂat morphology of uncinate pro- The focal left parietal SAH (Fig 1) correlates with the primarycesses, elastic paraspinal ligaments, and anterior wedge-like site of impact (ie, coupe injury), and the focal left frontal SDHmorphology of the vertebral bodies.13 These factors account may be consistent with contracoupe injury. Further hemor-for the relative ease of vertebral subluxation with complete rhage may be related to the coagulopathy as supported byrecovery of the bony elements to normal anatomical align- laboratory ﬁndings. This is a known phenomenon that mayment. This predisposes the child to cervical cord injury in the be initiated by tissue injury caused by trauma or hypoxiaabsence of bony abnormalities. Instantaneous damage to the ischemia.44,45 Once the capillary beds are open and leaking,respiratory centers at the cervicomedullary junction corre- further increases in ICP from brain edema and CPR maylated with the child’s respiratory distress, and subsequent exacerbate this process. Geddes et al32 suggest that additionalHIE lead to extensive edema and increased intracranial pres- factors such as venous and arterial hypertension (HTN) maysure (ICP). exacerbate hemorrhage in the ischemic, swollen brain with increased ICP. They propose both increased oozing from hypoxic veins in the setting of venous HTN secondary toHypoxic-Ischemic severe edema and increased hemorrhage from episodic orVersus Traumatic Axonal Injury sustained arterial HTN (eg, with reperfusion) that may occurGross and microscopic examination showed the effects of as a part of Cushing’s triad or be neurogenic in origin. Addi-severe HIE. There was no evidence of “primary” traumatic tionally, choking, vomiting, or paroxysmal coughing (eg,axonal injury (ie, TAI or shear injury) as an indicator of pertussis) may also result in SDH and RH.46-48 Furthermore,rotational acceleration-deceleration trauma to the brain. The the distribution of SDH or SAH along the interhemisphericprimary injury (ie, TAI) was shown to occur only at the ﬁssure is not pathognomonic for NAI, as previously reported,cervicomedullary junction. In cases of TAI (formerly “diffuse and has been shown to occur in cases of accidental traumaaxonal injury”), distinctive discrete swellings of the the ax- and HIE.14,16,17,21ons, known as axon bulbs, are observed microscopically onB-APP immunoperoxidase stains. These are focal or multifo- RHcal lesions and most often occur along deep gray/white mat- The initial funduscopic documentation of RH was not madeter junctions, the corpus callosum, and dorsal corticospinal until the child was in the PICU. Given the course of events totracts. They may also be associated with focal hemorrhage. that point, the RH may be a result of multiple factors asHIE, whether primary or secondary, results in a diffuse pat- described earlier regarding SDH and SAH. RH is a knowntern of axonal alteration. Furthermore, the histological ap- manifestation of increased ICP. There is no single type orpearance is different from that of TAI, forming a linear or pattern of RH that is pathognomonic of NAI/SBS, and RH isstreak pattern on B-APP staining.30-32 reported in a number of other conditions.15,16,49-57
Traumatic spinal cord injury 183Thoracic Spinal InjuryThe multiple thoracic compression fractures in this case areunusual in NAI (SBS) and require biomechanical assessment aswell as consideration of patient risk factors. Based on studies ofcompression fracture in intact cadavers subjected to ﬂexion andcompression testing of both adult human58,59 and pediatric ba-boon vertebral bodies,60 the biomechanical analysis suggestedthe presence of sufﬁcient force to cause the thoracic fractures, inaddition to the cervical spinal cord injury in this case. Additionally, the patient had steroid-dependent asthmatreated with daily beclomethasone dipropionate inhaler for aperiod of 8 months before the fall. During multiple visits tothe emergency room for exacerbations before the reportedfall, he also received additional doses of steroids in a form ofprednisone. Two weeks before the fall, he received 20 mg ofprednisone daily for 6 days. The inﬂuence of steroids in thiscase is uncertain. However, such high daily doses of oralsteroids have been shown to signiﬁcantly increase the risk offractures.61-63 Van Staa et al61 also showed that high dailydoses independent of duration of treatment or prior exposureput the patients at high risk for fractures. The patient also Figure A1 (See appendix). (Color version of ﬁgure is available on-presented to the emergency room 3 months before the cur- line.)rent incident after a fall down the stairs. He was evaluatedclinically and released. No imaging was performed at thattime. The postmortem histological examination of the verte-bral column showed evidence of acute trauma. Additionally, is the subsequent free-fall distance of the body CG to thean unusual distribution of diffuse microfractures was ob- ﬂoor.served in all bones examined, supporting the possible effect ● Using impulse momentum and assuming a triangularof chronic steroid therapy on bone fragility. It was impossible force pulse and plastic impact, peak force at impactto assess for bone density of the spine during necropsy be- F 2mv , where m is the mass of the object, v iscause the bones were decalciﬁed. impact velocity, and is the duration of impact. ● Compression force on lumbar vertebrae, Fv, is deter- mined by satisfying M I about the ligament attach-Conclusion ment point, as shown in the free-body diagram. Mo-Physicians have an obligation to completely and timely eval- ment-arm distances were scaled from values used byuate suspected NAI, including its mimics. The imaging ﬁnd- Myklebust et al.58ings alone cannot distinguish NAI from AI or from the med-ical mimics. A complete and thorough medical evaluation, Referencesusing evidence-based medicine principles, is necessary in 1. Donohoe M: Evidence-based medicine and shaken baby syndrome partparallel with the child-protection assessment. A multidisci- I: Literature review, 1966-1998. Am J Forensic Med Pathol 24:239-plinary approach to this evaluation is also important, includ- 242, 2003ing the involvement of qualiﬁed specialists. Such an ap- 2. Leestma J: Case analysis of brain injured admittedly shaken infants, 54proach may be the difference between appropriate child cases 1969-2001. Am J Forensic Med Pathol 26:199-212, 2005 3. Lyons: Shaken Baby Syndrome: A Questionable Scientiﬁc Syndromeprotection versus the improper breakup of a family or a and a Dangerous Legal Concept. Utah Law Rev 1109, 2003wrongful indictment and conviction. 4. Gena M” Shaken baby syndrome: Medical uncertaintly casts doubt on convictions. Wisc Law Rev 701, 2007 5. Le Fanu J: Wrongful diagnosis of child abuse—A master theory. J R SocAppendix Med 98:249-254, 2006 6. Mackey M: After the Court of Appeal: R v Harris and others Equations Used in Biomechanical Analysis EWCA crim 1980. Arch Dis Child 91:873-875, 2006 ● Angular velocity of combined chair-child system at end 7. Richards P, Bertocci G, Bonshek R, et al: Shaken baby syndrome. Before of inverted pendulum phase was determined as the court of appeal. Arch Dis Child 91:205-206, 2006 8. Baath J: Shaken baby syndrome: The debate rages on U. Toronto Med J 2 g L 1 cos , where L is height of combined 83:22-23, 2005 system center of mass and is angle of rotation from 9. Squier W: Shaken baby syndrome: The quest for evidence. Develop vertical position (Fig A1). Med Child Neurol 50:10-14, 2008 ● From conservation of energy, impact velocity v 10. Gilliland MGF: Use of the triad of scant SDH, brain swelling, and retinal hemorrhages to diagnose non-accidental injury is not scientiﬁcally v2 2gH where vz is the vertical component of linear z valid. National Association of Medical Examiners National Meeting, velocity at the end of the inverted pendulum phase and H October 2006 (abstr 53)
184 Barnes et al11. David TJ: Non-accidental head injury—The evidence. Pediatr Radiol 36. Weber W: Biomechanical fragility of the infant skull. Z Rechtsmed 38:S370-S377, 2008 (suppl 3) 94:93-101, 198512. Jaspan T: Current controversies in the interpretation of non-accidental 37. Goldsmith W, Monson KL: On the state of head injury biomechanics— head injury. Pediatr Radiol 38:S378-387, 2008 (suppl 3) Past, present, and future. Part 2: Physical experimentation. Crit Rev13. Pang D, Wilberger JE Jr: Spinal cord injury without radiographic ab- Biomed Eng 33:105-207, 2005 normalities in children. J Neurosurg 57:114-129, 1982 38. Plunkett J: Fatal pediatric head injuries caused by short-distance falls.14. Tung GA, Kumar M, Richardson RC, et al: Comparison of accidental Am J Forensic Med Pathol 22:1-12, 2001 and nonaccidental traumatic head injury in children on noncontrast 39. Gardner HB: A witness short fall mimicking presumed shaken baby computed tomography. Pediatrics 118:627-633, 2006 syndrome (inﬂicted childhood neurotrauma). Pediatr Neurosurg 43:15. Christian CW, Taylor AA, Hertle RW, et al: Retinal hemorrhages caused 433-435, 2007 by accidental household trauma. J Pediatr 135:125-127, 1999 40. Bandak FA: Shaken baby syndrome: A biomechanics analysis of injury16. Steinbok P, Singhal A, Poskitt K, et al: Early hypodensity of computed mechanisms. Forensic Sci Int 151:71-79, 2005 tomographic scan of the brain in an accidental pediatric head injury. 41. Margulies S, Prange M, Myers BS, et al: Shaken baby syndrome: A Neurosurgery 60:689-695, 2007 ﬂawed biomechanical analysis. Forensic Sci Int 164:278-279, 200517. Vinchon M, Noule N, Tchofo PJ. Et al. Imaging of head injuries in 42. Bandak FA: Author’s reply to “shaken baby syndrome: A ﬂawed bio- infants: temporal correlates and forensic implications for the diagnosis mechanical analysis.” Forensic Sci Int 164:282-283, 2005 of child abuse. J Neurosurg 101:44-52, 2004 43. Prange MT, Coats B, Duhaime AC, et al: Anthropomorphic simulations18. McNeeley PD, Atkinson JD, Saigal G, et al: Subdural hematomas in of falls, shakes, and inﬂicted impacts in infants. J Neurosurg 99:143- infants with benign enlargement of the subarachnoid spaces are not 150, 2003 pathognomonic for child abuse. AJNR Am J Neuroradiol 27:1725- 44. Hymel KP, Abshire TC, Luckey DW, et al: Coagulopathy in pediatric 1728, 2006 abusive head trauma. Pediatrics 99:371-375, 199719. Sirotnak AP: Medical disorders that mimic abusive head trauma, in 45. Miner KE, Kaufman HH, Graham SH, et al: Disseminated intravascular Frasier L, Rauth-Farley K, Alexander R, et al (eds): Abuse Head Trauma coagulation ﬁbrinolytic syndrome following head injury in children: in Infants and Children (ed 1). St Louis, MO, GW Medical Publishing, Frequency and prognostic implications. J Pediatr 100:687-691, 1982 2006, pp 191-248 46. Geddes JF, Talbert DG: Paroxysmal coughing, subdural and retinal bleeding: A computer modeling approach. Neuropathol Appl Neuro-20. Hymel KP, Jenny C, Block RW: Intracranial hemorrhage and rebleeding biol 32:625-634, 2006 in suspected victims of abuse head trauma: Addressing forensic con- 47. Talbert DG: Paroxysmal couph injury, vascular rupture and ‘shaken troversies. Child Maltreat 7:329-348, 2002 baby syndrome.’ Med Hypotheses 64:8-13, 200521. Barnes PD, Krasnokutsky MV: Imaging of the central nervous system in 48. American Academy of Pediatrics red book online. Pertussis. Available suspected or alleged nonaccidental injury, including the mimics. Top at: http://www.aapredbook.aappublications.org/cgi/content/extract/ Magn Reson Imaging 18:53-74, 2007 2006. Accessed November 200822. Twoney EL, Iemsawatdikul K, Stephens BG, et al: Multiple thoracic 49. Lantz PE, Sinal SH, Stanton CA, et al: Perimacular retinal folds from vertebral compression fractures caused by non-accidental injury: Case childhood head trauma. BMJ 328:754-756, 2004 report with radiologicalpathological correlation. Pediatr Radiol 34: 50. Ebube O, Watts P: Are there any pathognomonic signs in shaken baby 665-668, 2004 syndrome? J AAPOS 11:99-100, 2007 (abstr)23. Sane SM, Kleinman PK, Cohen RA: American Academy of Pediatrics. 51. Goetting MG, Sowa B: Retinal hemorrhage after cardiopulmonary re- Section on Radiology Diagnostic imaging of child abuse. Pediatrics suscitation in children: An etiologic reevaluation. Pediatrics 85:585- 105:1345-1348, 2000 588, 199024. Ahmann PA, Smith SA, Schwartz JF, et al: Spinal cord infarction due to 52. Lantz PE, Stanton CA: Postmortem Detection and Evaluation of Retinal minor trauma in children. Neurology 25:301-307, 1975 Hemorrhages. Seattle, WA, American Academy of Forensic Sciences, 200625. Riviello JJ, Marks HG, Faerber EN, et al: Delayed cervical central cord 53. Lueder GT, Turner JW, Paschall R: Perimacular retinal folds simulating syndrome after trivial trauma. Pediatr Emerg Care 62:113-117, 1990 nonaccidental injury in an infant. Arch Ophthalmol 124:1782-1783,26. Chen LS, Blaw ME: Acute central cervical cord syndrome caused by 2006 minor trauma. J Pediatr 108:96-97, 1986 54. Gilles EE, McGregor ML, Levy-Clarke G: Retinal hemorrhage asymme-27. Cheshire DJ: The paediatric syndrome of traumatic myelopathy with- try in inﬂicted head injury: A clue to pathogenesis? J Pediatr 143:494- out demonstrable vertebral injury. Paraplegia 15:74-85, 1977 499, 200328. Launay F, Leet AI, Sponseller PD: Pediatric spinal cord injury without 55. Obi E, Watts P: Are there any pathognomonic signs in shaken baby radiographic abnormality: A meta-analysis. Clin Orthop Relat Res 433: syndrome? J AAPOS 11:99-100, 2007 166-170, 2005 56. Brown S, Levin AV, Ramsey D, et al: Natural animal shaking: A model29. Brown RL, Brunn MA, Garcia VF: Cervical spine injuries in children: a for inﬂicted neurotrauma in children? J AAPOS 11:85-86, 2007 review of 103 patients treated consecutively at a level 1 pediatric 57. Binenaum G, Forbes BJ, Raghupathi R, et al: An animal model to study trauma center. J Pediatr Surg 36:1107-1114, 2001 retinal hemorrhages in nonimpact brain injury. J AAPOS 11:84-85, 200730. Geddes JF, Vowles GH, Hackshaw AK: Neuropathology of inﬂicted 58. Myklebust J, Sances AJ, Maiman DJ, et al: Experimental spinal trauma head injury in children I. Patterns of brain damage. Brain 124:1290- studies in the human and monkey cadaver, in Proceedings of Stapp Car 1298, 2001 Crash Conference. October 1983, San Diego, CA. 1983:149-16131. Geddes JF, Vowles GH, Hackshaw AK: Neuropathology of inﬂicted 59. Yamada H: Strength of Biological Materials. Baltimore, MD, Williams head injury in children II. Microscopic brain injury in infants. Brain and Wilkins, 1970 124:1299-306, 2001 60. Nuckley DJ, Eck MP, Carter JW, et al: Spinal maturation affects verte-32. Geddes JF, Tasker RC, Hackshaw AK, et al: Dural haemorrhage in bral compressive mechanics and BMD with sex dependence. Bone 35: non-traumatic infant deaths: does it explain the bleeding in ‘shaken 720-728, 2004 baby syndrome’? Neuropathol Appl Neurobiol 29:14-22, 2003 61. Van Staa TP, Leufkens HGM, Abenhaim L, et al: Oral corticosteroids33. Snyder RG, Schneider LW, Owings CL, et al: Anthropometry of infants, and fracture risk: Relationship to daily and cumulative doses. Rheuma- children, and youths of age 18 for product safety design. Final report. tology 39:1383-1389, 2000 Consumer Product Safety Commission. UM-HSRI-77-17, May 31, 1977 62. Yen D, Hedden D: Mutiple vertebral compression fractures in a patient treated34. Prange M, Luck J, Dibb A, et al: Mechanical properties and anthropom- with corticosteroids for cystic ﬁbrosis. Can J Surg 45:383-384, 2002 etry of the human infant head. Stapp Car Crash J 48:279-299, 2004 63. Makitie O, Doria A, Henriques F, et al: Radiographic vertebral mor-35. Weber W: Experimental studies of skull fractures in infants. Z Re- phology: A diagnostic tool in pediatric osteoporosis. J Pediatr 146:395- chtsmed 92:87-94, 1984 401, 2005